The mobilization of FFA from adipose tissue can be considered, in general terms, to be a two step process. First, FFA are produced by hydrolysis of triglycerides (lipolysis) and secondly, FFA exit the adipocyte into the extracellular fluid. Although considerable experimental attention has been given to understanding the control of lipolysis, very little is known about the cellular mechanisms by which FFA leave adipocytes. One objective of this research is to test the hypothesis that cytoplasmic microtubules are somehow involved in mobilization of FFA from adipocytes. In support of this theory are the findings that treatment of adipose tissues with colchicine, vinca alkaloids or podophyllin, agents which disrupt microtubules, impairs mobilization of FFA. The site of action of colchicine on adipose tissue has been localized to a non-sedimentable protein having a molecular weight of 120,000, a sedimentation coefficient of 5.9 S and which is similar to the protein subunit of microtubules, called tubulin. However, the precise role that this protein plays in lipid mobilization remains unclear. Because most studies have shown that microtubule-dependent processes also require calcium ion, experiments on the role of calcium ion in control of lipid mobilization were performed. These studies indicated that calcium was indeed required for lipid mobilization but that it acted at a site antecedent to hydrolysis of triglycerides, perhaps by facilitation hormonal activation to adenylate cyclase.